Protective effect of gossypol on lipopolysaccharide-induced acute lung injury in mice

• Published in: Inflammation research 2013-05, Vol.62 (5), p.499-506
• Main Authors: Liu, Zhicheng, Yang, Zhengtao, Fu, Yunhe, Li, Fenyang, Liang, Dejie, Zhou, Ershun, Song, Xiaojing, Zhang, Wen, Zhang, Xichen, Cao, Yongguo, Zhang, Naisheng
• Format: Article
• Language: English
• Subjects: Acute Lung Injury - chemically induced; Acute Lung Injury - drug therapy; Acute Lung Injury - metabolism; Acute Lung Injury - pathology; Allergology; Animals; Anti-Inflammatory Agents - pharmacology; Anti-Inflammatory Agents - therapeutic use; Biomedical and Life Sciences; Biomedicine; Bronchoalveolar Lavage Fluid - chemistry; Bronchoalveolar Lavage Fluid - cytology; Cell Count; Cytokines - metabolism; Dermatology; Gossypol - pharmacology; Gossypol - therapeutic use; Immunology; Lipopolysaccharides; Male; Mice; Mice, Inbred BALB C; Mitogen-Activated Protein Kinases - metabolism; Neurology; NF-kappa B - metabolism; Original Research Paper; Peroxidase - metabolism; Pharmacology/Toxicology; Rheumatology
• ISSN: 1023-3830; 1420-908X
• DOI: 10.1007/s00011-013-0603-6

Objective Gossypol has been reported to have anti-inflammatory properties. The purpose of this study was to evaluate the effect of gossypol on acute lung injury (ALI) induced by lipopolysaccharide (LPS) in mice. Methods Male BALB/c mice were pretreated with gossypol 1 h before intranasal instillation of LPS. Then, 7 h after LPS administration, the myeloperoxidase in histology of lungs, lung wet/dry ratio and inflammatory cells in the bronchoalveolar lavage fluid (BALF) were determined. The levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and interleukin-1β (IL-1β) in the BALF were measured by ELISA. The extent of phosphorylation of IκB-α, p65 NF-κB, p46–p54 JNK, p42–p44 ERK, and p38 were detected by western blot. Results Gossypol markedly attenuated the LPS-induced histological alterations in the lung and inhibited the production of TNF-α, IL-1β and IL-6. Additionally, gossypol reduced the inflammatory cells in BALF, decreased the wet/dry ratio of lungs and inhibited the phosphorylation of IκB-α, p65 NF-κB, p46–p54 JNK, p42–p44 ERK, and p38 caused by LPS. Conclusion The data suggest that anti-inflammatory effects of gossypol against the LPS-induced ALI may be due to its ability of inhibition of the NF-κB and MAPKs signaling pathways. Gossypol may be a promising potential therapeutic reagent for ALI treatment.